PART A READING

Wood Dust Allergies

TIME LIMIT 15 MINUTES

Read the following reading material about wood dust allergies.

You only have 15 minutes to scan the reading materials then fill in the
synthesizing exercise (last page) – so only skim and scan read the reading
material – do not spend a lot of time reading it in depth.

NOTE: This Part A exercise has five (not four) reading texts - and 27 (not the usual 30)
gaps to fill in. It is suggested that if you correctly complete 65% of the 27 gaps in 17
minutes – this would equate with the OET “B” pass mark.

In the exercise on the last page – fill in the missing word (or words) – using one, two or
three word-answers, depending on the number of indicated spaces to be filled in.
WOOD DUST ALLERGIES
READING TEXT # 1 -EXPOSURE TO TOXIC DUST

Workers may come into contact with many forms of toxic dust ranging from
crystalline silica to wood dust and nanoparticles. This chapter provides an overview
of the health impacts of exposure to respirable crystalline silica, beryllium, wood
dust, alumina and textile dusts. The emerging issue of nanoparticle hazards is
discussed in the following pages

Exposure to respirable crystalline silica (RCS) occurs through cutting, chipping,

drilling or grinding objects containing crystalline silica or through the use of materials
that contain crystalline silica for abrasive blasting, for example sandblasting.

Workers in many occupations and industries use and come into contact with
materials containing crystalline silica, contact occurring through

• excavation, where dust is created by drilling, chipping, jackhammering, etc;

• cutting to size of bricks, blocks, lightweight concrete panels, tiles, etc;
• sandblasting;
• grinding of floor slabs, granite for decorative purposes;
• concrete cutting and drilling;
• road building;
• glass manufacturing;
• refractory bricklaying;
• demolition; and
• sweeping concrete floor slabs.
WOOD DUST ALLERGIES
READING TEXT # 2 -NUMBERS OF WORKERS EXPOSED

The number of workers potentially exposed to silica in the course of their work was
reported by the National Occupational Health and Safety Commission (NOHSC) as
nearly 294 000 in 2002.

NOHSC noted that ’it should be kept in mind that workers in some of these
industries have a different likelihood of exposure compared to those in others, that
not all workers in the same industry will have the same likelihood of exposure, and
the different exposed workers are likely to be exposed to different levels of silica’.

Exposure to crystalline silica is known to cause a number of diseases and is linked to

others.

Silicosis has long been known as a disease associated with mining and is caused by
the inhalation of dust containing crystalline silica. Silicosis is characterised by a
diffuse, nodular, interstitial pulmonary fibrosis. Silicosis may cause breathing
difficulties, chest pain, respiratory failure and lead to death. There are three main
types of silicosis:

• Chronic/classic silicosis, which is the most common type, occurs after 15-20 years
of moderate to low exposure. Worker may experience shortness of breath
upon exercising. In the later stages the worker may experience extreme
shortness of breath, chest pain or respiratory failure.

• Accelerated (subacute) silicosis, can occur after 5-10 years of exposure to high
levels of silica. Symptoms include severe shortness of breath, weakness
and weight loss. The onset of symptoms takes longer than in acute silicosis.

• Acute silicosis, occurs after a few months or as long as two years following
exposure to extremely high concentrations of respirable crystalline silica.
Symptoms include severe disabling shortness of breath, weakness and
weight loss, which often leads to death.
WOOD DUST ALLERGIES
READING TEXT # 3 -LATENCY OF CHRONIC SILICOSIS

The fatal course of the disease is not influenced by treatment. This disease is
primarily reported in occupations that can have very high exposures to fine silica
dusts and include sandblasters, stone crushers, ceramic workers and workers in
abrasive manufacturing.

There was extensive discussion in evidence on the latency of chronic silicosis.

Cement Concrete and Aggregates Australia (CCAA) stated that chronic silicosis has a
latency that may be up to seven years after cessation of exposure: ’that is, a worker
may have no symptoms or signs of silicosis either clinical or on chest X-ray at the
time of cessation of exposure and then be diagnosed with clinical silicosis up to
about seven years later, with little or no clinical evidence of disease in the
intervening period (and no ongoing exposure)’.

CCAA went on to state that this delayed appearance or latency is rare and ’probably
95 per cent of all cases of silicosis are diagnosable within a year of cessation of
exposure, if not at the time of exposure’. CCAA commented:

The evidence from the literature is that nearly all workers who will eventually be
diagnosed as having silicosis are diagnosable at the time their exposure ceases.
Some who cease work because they are unwell, or leave work without having a
recent X-ray, may not actually be diagnosed until they are investigated, but this
usually occurs in a short period after they report illness to their doctor. If they
have been under surveillance in compliance with the Hazardous Substances
Regulations governing crystalline silica (in all Australian jurisdictions) they should
have had an X-ray within 5 years of ceasing exposure. It can be expected that
almost all who will eventually be diagnosed as having silicosis will have evidence
on those X-rays.

CCAA stated that silicosis does not have a long latency period, comparable with
mesothelioma (which may occur up to 40 years after exposure has ceased) or some
other occupational cancers. Those workers whose X-ray is classed as ’no opacities’
when they cease exposure, will rarely develop opacities (with or without any signs of
silicosis) in later years. CCAA concluded ’latency is not a major issue in relation to
silicosis, and there will not be a wave of hidden cases occurring years ahead. The few
who do will develop those opacities within a short time of ceasing work.’
WOOD DUST ALLERGIES
READING TEXT # 4 -AIRWAY DISEASE and LUNG CANCER
AIRWAY DISEASE
- While silicosis has long been identified
as an occupational disease arising from
inhalation of dust containing crystalline
silica, there has been some dispute over
the association of airway disease with
crystalline silica.
- There has been extensive discussion in
evidence as to the incidence of airway
disease related to toxic dust
- Chronic obstructive pulmonary disease
(COPD) refers to a combination of cough
and phlegm, breathlessness and airflow
obstruction. Professor E Haydn Walters,
University of Tasmania, stated that
generally, ’it is likely that somebody will
go from having some irritant cough and a
bit of sputum to gradually developing
some airflow obstruction to then
becoming symptomatic and breathless
on exercise perhaps over a 15- to 20-year
period if they have moderate dust
exposure which is continuing’.
- There was also a view that exposure to
silica and other toxic dust causes lung
parenchymal fibrosis or silicosis and not
airway disease.
LUNG CANCER
Since 1997 silica has been listed as a
Class One carcinogen by the
International Agency for Research on
Cancer (IARC).
In 2002 NIOSH commented that ’the
carcinogenicity of crystalline silica in
humans has been strongly debated in the
scientific community’.
The NOHSC Regulation Impact Statement
(2004) stated that ’the balance of
evidence suggests that RCS exposure
causes lung cancer’ but that ’there is
dispute as to whether RSC exposure
causes lung cancer directly, or
whether RCS exposure causes lung
cancer indirectly, i.e., whether the
development of silicosis increases the
risk of lung cancer’.
The Regulation Impact Statement
provided the following comparison of
carcinogen classifications of crystalline
silica.
- Crystalline silica . human
carcinogen
- Crystalline silica . potential
occupational carcinogen
- RCS . known to be a human
carcinogen
- RCS . causes lung cancer, but is
probably a weak carcinogen
- Crystalline silica . suspected
human carcinogen
WOOD DUST ALLERGIES

READING TEXT # 5 -GLOBAL EVIDENCE

-A literature review by the UK Institute for Environment and Health concluded

that the literature suggested there are clearly elevated risks of developing COPD
associated with several occupations including welding, flour mill work and cotton
textile work.

-The US National Institute for Occupational Safety and Health (NIOSH) published a
hazard review on RCS in 2002. It concluded that silica is one of a number of
occupational dusts associated with COPD. The review also noted that some studies
suggest these diseases may be less frequent or absent in non-smokers.

-In 1999 British miners were recognised as suffering a high incidence of COPD in
relationship to mineral dust exposure, even in the absence of classic Coal Workers’
Pneumoconiosis (CWP). Subsequently, the British Government assessed miners
and ex-miners and provided compensation.

-The Australian Institute of Occupational Hygienists (AIOH) also commented on

airway disease and noted that it has been statistically associated with some
occupational groups such as miners who may have been exposed to long term high
dust exposures. It commented that: The findings are controversial as the
associated disease symptoms are confounded due to lifestyle factors, particularly
tobacco smoking. Similar to the findings with lung cancer outcomes, for airways
disease detailed examination of the various risk factors indicates that tobacco
smoking contributes a higher risk component and hence the majority of the case
numbers.

-The AIOH also noted that in its Regulation Impact Statement on the Proposed
Amendment to the National Exposure Standards for Crystalline Silica in October
2004, the Committee stated emphysema, the main cause of chronic obstructive
lung disease, can be caused by inhalation of crystalline silica and that silica dust can
worsen the damage done by smoking.
PART A READING -WOOD DUST ALLERGIES SYNTHESISING EXERCISE

Silicosis, a respiratory disease caused by exposure to crystalline silica, has a history of

being associated with ………………………….. 1 . Toxic dust reaches workers in a variety of ways:
cutting, chipping, drilling or grinding objects or even …………………………….. 2
Toxic dusts occurs in the form of ………………………….. ……………………….. 3 , wood dust and
even …………………………… 4 . Common contact occupations include road building,
…………………………. 5 manufacture and excavation work where dust results from
jackhammering, drilling and ……………………… 6 .

In Reading 2 we find that nearly ……………………… 7 workers in 2002 were possibly exposed to
silica during their working hours. According to the NOHSC, not ……… 8 workers in one
particular industry have the same exposure risk. The NOHSC also reported that individuals
are likely to be exposed to …………………. …………………… 9 of silica.
There are three main types of Silicosis: ……………………. 10 or classic silicosis, accelerated or
………………………….. 11 silicosis and ……………………… 12 silicosis. The common symptom is
…………………… …………. ………………….. 13.

The UK and US literature reports that development of COPD is associated with …………….. 14
dusts. The NIOSH noted that in some of its research, respiratory illness may be less
frequent or ………………….. 15 in …… ………………….16 . In 1999, the British Government
awarded ……………………….. 17 to British miners who were found to be suffering a high
…………………………… 18 of COPD in ratio to their ……………………. 19 dust exposure.

So is there any evidence that occupational dust causes lung cancer or disease of the
airways? One view is that exposure to toxic dusts causes ……………. 20 but not airway
disease. However, since ………………. 21, silica has been listed as a Class 1 carcinogen
and in ……………… 22 an impact statement ruled that RCS exposure …………………..
…………….… …………………….23 .

According to a Tasmanian researcher, COPD develops over a ……. to ….… 24 year period if
the sufferer has ……………………… 25 exposure to moderate dust levels. It seems the debate is
set to run for a number of years yet: the Committee in 2004 stated …………………….. 26 ,
recognised as the main cause of COPD , may be caused by breathing in silica dust but that
the likelihood of developing the disease was exacerbated by …………………… 27 .
PART A – WOOD DUST ALLERGIES - ANSWERS

Q3 crystalline Q4
Q1 mining Q2 sandblasting Q5 glass
silica nanoparticles

Q9 different
Q6 chipping Q7 294,000 Q8 all Q10 chronic
levels

Q13 shortness Q14

Q11 subacute Q12 acute Q15 absent
of breath occupational

Q16 non Q17

Q18 incidence Q19 mineral Q20 silicosis
smokers compensation
Q23 causes lung
Q21 1997 Q22 2004 Q24 15 to 20 Q25 continuous
cancer
Q26
Q27 smoking
Emphysema